Managing the Patient with Psoriasis and Metabolic Comorbidities

Abstract

Epidemiological data demonstrate strong associations between psoriasis and metabolic comorbidities, including obesity, hypertension, diabetes mellitus, dyslipidemia, and non-alcoholic fatty liver disease. The presence of metabolic comorbidities significantly influences the selection and effectiveness of pharmacological treatments. Some drugs should be prescribed with caution in patients with metabolic comorbidities because of an increased risk of adverse events, while others could have a reduced effectiveness. The aim of this narrative review is to highlight the challenges that healthcare professionals may face regarding the management of psoriasis in patients with metabolic comorbidities. In the first part of the article, the epidemiological association between psoriasis and metabolic comorbidities and their pathogenetic mechanisms is summarized. The second part describes the efficacy and safety profile of conventional and biologic drugs in patients with selected metabolic comorbidities including obesity, non-alcoholic fatty liver disease/hepatic steatosis, and diabetes. Finally, the role of pharmacological and non-pharmacological interventions, such as diet, alcohol abstinence, physical activity, and smoking avoidance is discussed. In conclusion, the choice of the best approach to manage patients with psoriasis with metabolic comorbidities should encompass both tailored pharmacological and individualized non-pharmacological interventions.

Fig. 1

Cross-talk between psoriatic lesions and liver, adipose, and muscular tissue involving different mediators (i.e., adipokines, tumor necrosis factor [TNF]-α, interferon [IFN]-α, [IFN]-γ, interleukin [IL]-1, IL-6, and IL-17) that stimulate the production of homocysteine, C-reactive protein, and fibrinogen from the liver; chemerin, leptin, resistin, triglycerides, and low-density lipoprotein (LDL)-cholesterol from the adipose tissue; and promote insulin resistance in the skeletal muscle. These mediators could promote endothelial dysfunction and atherogenesis